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The role of small heat-shock protein αB-crystalline (HspB5) in COPD pathogenesis

Authors Cherneva R, Georgiev O, Petrova D, Trifonova NL, Stamenova M, Ivanova V, Vlasov

Received 11 June 2012

Accepted for publication 2 August 2012

Published 4 October 2012 Volume 2012:7 Pages 633—640

DOI https://doi.org/10.2147/COPD.S34929

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 2


Radostina V Cherneva,1 Ognian B Georgiev,1 Daniela S Petrova,1 Nedka L Trifonova,2 Maria Stamenova,2 Vesela I Ivanova,3 Veselin I Vlasov3

1Clinic of Internal Medicine, Division of Pulmonology, University Hospital Alexandrovska, Sofia, Bulgaria; 2Department of Biology, 3Department of Pathology, Medical University of Sofia, Sofia, Bulgaria

Background: αB-crystallin (HspB5) is a chaperone whose role as a marker of innate immunity activation as well as its therapeutic potential have recently been investigated in several inflammatory diseases: multiple sclerosis, myocardial ischemia, and Guillain–Barré syndrome.
Aim: The aim of this study is to determine the role of αB-crystallin in chronic obstructive pulmonary disease (COPD) pathogenesis and inflammation.
Materials: Plasma levels of αB-crystallin were studied in 163 patients: 52 healthy non-COPD smokers; 20 COPD smokers in Global Initiative for Chronic Obstructive Lung Disease (GOLD) stages I–II; 43 COPD smokers in GOLD stages III-IV. Forty-eight patients were diagnosed with acute inflammatory respiratory disease. The plasma levels of αB-crystallin antibodies were determined by an enzyme-linked immunosorbent assay (Calbiochem), and were confirmed with Western blotting. Tissue expression of the protein was compared in three different groups of patients: COPD smokers, COPD nonsmokers, and in patients with age-related emphysema.
Results: The mean level of anti-αB-crystallin antibodies in non-COPD smokers was 0.291nm. In COPD smokers it was 0.352 nm and, in patients with inflammatory lung diseases, 0.433 nm. in patients with inflammatory lung diseases. There was a statistically significant difference between COPD smokers and healthy non-COPD smokers (P = 0.010). The same could be observed comparing the group of patients with acute inflammation and non-COPD healthy smokers (P = 0.007). There was no statistically significant difference between patients with mild/moderate inflammation and those with severe COPD. Tissue detection of the protein showed that it was significantly overexpressed in COPD smokers in comparison to COPD nonsmokers and was only slightly expressed in patients with age-related emphysema.
Conclusion: αB-crystallin is increased in patients with inflammatory lung diseases. Though unspecific, it could be used in a panel of markers discerning COPD smokers from healthy nonsmokers. As αB-crystallin is a regulator of innate immunity and a therapeutic anti-inflammatory agent, its exact role in COPD pathogenesis and therapy should be explored further.

Keywords: COPD, HspB5, chaperonopathology, pathogenesis

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